Category Archives: Prehospital Trauma

Greg Brown returns to look at an important thing relevant to first responders (and lots of other people really) – the sucking chest wound.

We’ve all been there – sitting through some kind of “first aid” training and having some kind of “first aid trainer” speaking authoritatively on some kind of “first aid style” topic. If you are like me you’ve used your time productively over the years and perfected what my wife refers to as “screen-saver mode” – it’s that look on your face that tells the instructor that you are listening intently, often supplemented by the insertion of “knowing nods” or head-tilts, but in actual fact you are asking yourself “if I was able to collect all of my belly button lint over a 12 month period and spin it into yarn, I wonder if I could make enough to abseil off London Bridge?”

Don’t get me wrong – I reckon effective and accurate first aid training should be a mandatory part of having a car / bike / truck / bus licence. More appropriately trained people should mean faster recovery rates for most injured people (and less work for overstretched first responders).

It’s just that sometimes first aid trainers teach stuff based on ‘we reckon’ or ‘that’s how we’ve always done it’ rather than evidence or knowing it works in the real world. This post is about one of those things.

“What is a sucking chest wound?”

In the Army questions come in a few different shapes and sizes. A popular one is “there is only one obscure answer you should have guessed I wanted”. Trust me, the muzzle velocity of your primary weapon is 970 metres per second.

Another popular one is “the question that should be about one thing, but is actually to demonstrate a quite tangential point”. Like,

“What is a sucking chest wound?”

For an army instructor the answer is not what you are thinking right now. It is “Nature’s way of telling you that your field craft sucks and everyone can see you and now you got shot”.

Let’s Go With the Medical One

We’re going to go with the alternative, more medical one. A sucking chest wound is defined as air entering the thorax via a communicating wound that entrains air into the space between the lungs and ribs more readily than the lungs can expand via inspiration through the trachea.

This is about pressure differentials – in order to inhale, the lungs must generate a relative negative pressure such that air can be sucked into them via the trachea. But if you make a big communicating hole in the trachea, that might become a pretty big highway for air to enter the space with the negative pressure.

The communicating hole does need to be pretty big. Depending upon which textbook you read, this hole needs to be a minimum of a half to three quarters the diameter of the trachea. Also, the patient needs to be undergoing relative negative pressure ventilation (or, in simple terms, breathing spontaneously). If they are being artificially ventilated (which requires positive pressure) then the pressure inside the lungs will be higher than the pressure on the outside of the body; the result is that air will be forced out of the intra-pleural space (or thorax) by the expanding lung (as opposed to being entrained into the thorax via the hole in the chest).

Are sucking chest wounds really that bad?

Well, yes. They suck in fact.

A sucking chest wound creates what is known as an open pneumothorax. Let’s consider the option where that hole does not seal on expiration. We’ll get onto the also very annoying sealing with a flap version in a bit.

In this slightly not so annoying case, the patient will have a ‘tidalling’ of air in and out of this communicating hole. The effect? Respiratory compromise, increased cardiovascular effort and reduced oxygen saturations. Patient satisfaction? No, not really. Death? Maybe – depends on what other injuries exist and the ability of the individual to compensate. See Arnaud et al (2016) for more details.

But if this communicating hole were to seal itself on expiration then you now have an open tension pneumothorax. Sounds bad; IS bad.

In such a case, each time the patient breathes in they will entrain air through the communicating hole in the chest wall (that whole “negative pressure” thing in action). But when they breathe out, instead of having that additional intra-pleural air tidal outwards, the flap will seal it in place; each time they breathe in, the volume of trapped air will increase and you’ll end up with the tension bit.

How much air is required? Well a randomised, prospective, unblinded laboratory animal (porcine) trial conducted by Kotora et al (2013) found that as little as 17.5mL/kg of air injected into the intra pleural space resulted in a life-threatening tension effect.

Actually, that’s a fair bit of air…for those of you who are lazy and don’t want to do the math, that’s 1400mL for an 80kg person. But remember, any tension pneumothorax (open or closed) is progressive – each time you breathe, more air is trapped; therefore, it doesn’t take long to reach crisis levels.

“But are they common enough for us to be worried about?”, I hear you asking. The short answer is yes – in fact, the long answer is also yes.

Kotora et al (2013) reviewed the statistics from the Joint Theater Trauma Registry regarding contemporary combat casualties with tension pneumothorax and found that they accounted for 3 – 4% of all casualties, but 5 – 7% as the cause of lethal injury.

“Yes, but I don’t live in a combat zone…”, I hear you say. I have two responses:

Good for you; but also,

According to Littlejohn (2017), thoracic injury accounts for 25% of all trauma mortality. And sure that stat is for all forms of thoracic injury and a sucking chest wound is but one of those but there’s a neat article by Shahani which sums up the incidence nicely and it turns out you should give this some thought.

We even saved you some time by grabbing the relevant image.

So, your field craft sucks – now what?

Now that we know that sucking chest wounds are both possible and bad, we should probably discuss treatment.

Some History

Back in the mid 1990’s, Army instructors were very big on rigging up a three-sided dressing. Unwrap a shell dressing, turn the rubbery-plastic wrapper into a sheet and tape three sides down with the open bit facing the feet to allow blood drainage.

And, in an astonishing turn of events, everyone I’ve met who tried this confirmed it didn’t really work that well.

In that Littlejohn paper they make reference to the fact that by the 2004 ATLS guidelines (which are not usually that quick moving), it was being written unblock and white that there was no evidence for or against the three-sided dressing option. It was done because it sounded good in theory, but the evidence wasn’t there.

Now to the New

Actually, not that new. Chest seals already existed.

These chest seals (at that time the Bolin produced by H & H Medical, and the Asherman produced by Teleflex medical) included one-way valves to allow for the forced escape of trapped intrathoracic air and blood. basically they took the impromptu three-sided dressing and made it a ready-made device in the form of an occlusive dressing with an integral vent.

But did they work?

Yes and no.

On a perfectly healthy (albeit with a surgically created open pneumothorax) porcine model with cleaned, shaved, dry skin they sealed well and vented air adequately.

However, once the skin was contaminated (dry blood, dirt, hair etc) the Bolin sealed much better than the Asherman. And if there was active blood drainage too (such as in an open haemo-pneumothorax) then all bets were off. Both vents clogged with blood and ceased to work. Sure, you could manually peel the seal back and physically burp the chest but if you did so the Bolin became an un-vented seal and the Asherman was as good as finished (i.e. it wouldn’t reseal). But hey, at least you had sealed the communicating hole and in doing so stopped entraining air.

“Is this the best you can do?” you may be asking. Well to be honest, since the vents didn’t work for more than a breath or two most people decided that the vents were pointless. The outcome was that we all decided to forget about the vents and just seal the wound. That way, assuming that there was no perforation to the lung, this open tension pneumothorax (aka sucking chest wound) became a routine, run of the mill, plain old pneumothorax. And if there were signs of tensioning (e.g. increasing respiratory distress, hypotension, tachycardia….) one just needed to peel back the seal and manually burp the communicating hole thus relieving the pressure. Use a defib pad – those bad boys stick to anything! Problem solved….

Or how about a newer idea + research?

In 2012 the Committee on Tactical Combat Casualty Care (CoTCCC) started questioning the efficacy of contemporary practices regarding the placement of chest seals on sucking chest wounds. It had already been accepted that the current vented chest seals had ineffective vents, so practice had changed from using a chest seal with an ineffective vent to simple, “soldier proof” unvented seals and burping them as required. Surely there had to be a better way…?

What they found was that all three were effective in sealing around the surgically inflicted wounds and in evacuating both air and blood. Thus, in 2013, CoTCCC changed their recommendations back to the use of vented chest seals.

But there were still some questions:

Once life gets in its messy way, do they seal (or at least stick to skin)?

Are all vent designs equal?

To answer question 1, Arnaud et al (2016) decided to evaluate the adhesiveness of the 5 most common chest seals used in the US military using porcine models. What they found was that the Russell, Fast Breathe, Hyfin and SAM all had similar adherence scores for peeling (> 90%) and detachment (< 25%) when tested at ambient temperatures and after storage in high temperature areas when compared to the Bolin. The researchers admitted, though, that further testing was required to assess the efficiency of the seals in the presence of an open tension haemo-pneumothorax.

In response to question 2, Kheirabadi et al (2017) tested the effectiveness of 5 common chest seals in the presence of an open tension haemo-pneumothorax (again, on porcine models). Essentially, there are two types of vent: (i) ones with one-way valves (like in the Bolin and Sam Chest Seals), and (ii) ones with laminar valves (like in the Russell and Hyfin Chest Seals). Their question was: do they both work the same?

What they found was that when the wound is oozing blood and air then seal design mattered. They found that the seals with one-way valves (specifically the SAM and Bolin) had unacceptably low success rates (25% and 0% respectively) because the build-up of blood either clogged the valve or detached the seal. By contrast, seals with laminar venting channels had much higher success rates – 100% for the Sentinel and Russell, and 67% for the Hyfin.

The Summary

So:

Sucking chest wounds are bad for your health.

Sealing the wound is good.

If the seal consistently allows for the outflow of accumulated air and blood, then that’s even better.

Therefore, now that we know all of this, one’s choice of chest seal is important. At CareFlight we use the Russell Chest Seal by Prometheus Medical (and no, we’re not paid to mention them we’re just sharing what we do). Why? Because it works – consistently. Both for us and in all the aforementioned trials.

The premise of this addition to the Collective is that you’re a first responder. That being the case, use an appropriate vented chest seal on a sucking chest wound.

However, you still need to recognise that the placement of the seal does not automatically qualify you for flowers and chocolates at each anniversary of the patient’s survival – you still need to monitor for and treat deterioration. Such deterioration is likely to include a tension pneumothorax for which the treatment is outside of the scope of most first responders (other than burping the wound).

If you are a more advanced provider then your treatments might include the performance of a needle thoracocentesis, or perhaps intubation with positive pressure ventilation and a thoracostomy (finger or tube).

In essence, know the signs and symptoms then master the treatments that are inside your scope of practice. (Or you could enrol in a course…such as CareFlight’s Pre-Hospital Trauma Course or even THREAT… OK that was pretty shameless.)

Meanwhile we’d love to hear:

What chest seal do you use?

Why?

How does it go?

Or you could just tell us what other things you think suck.

Could be the leafy green thing. Could be a person maybe.

Notes:

We’re not kidding about hearing back from you. Chip in. It only helps to hear other takes.

You could also consider sharing this around. Or even following along. The signup email thing is around here somewhere.

That image disparaging all things Kale (or kale) is off the Creative Commons-type site unsplash.com and comes via Charles Deluvio without any alterations.

There are parts of the resuscitation with no algorithm. No protocol. How do we improve that part? What are the social resuscitation skills we need to work on? We’re very pleased to have Dr Ruth Parsell chip in with some thoughts. Ruth is a current ACEM Registrar working on the CareFlight Rapid Response Helicopter in Sydney. She joined the NSW Ambulance Service in 1998 and has worked in prehospital and hospital settings in varying roles since that time.

The “social” resuscitation is a term I’ve been using for quite some time now. I apply it in dire situations. In both adults and children. But this is about the paediatric resuscitation and, specifically, cases where the prognosis is highly likely to be tragic. It is in these cases that I utilize this term because we are clearly treating more than just the patient when we resuscitate. I use the term because when I treat the child I am treating their family and all of the social connections that are linked to such a brief, precious life.

Experience We Don’t Always Want to Gain

The sad reality is that every paediatric resuscitation we do offers an opportunity to improve more than just our clinical skills. We all wish we didn’t see these cases but if they continue to occur then we will continue to do our best to serve the needs of both the patients and their families. What if we were able to improve the way we serve them? Which part of the resuscitation we call “futile” is the opposite of futile?

The best way to do both would be to have the “miracle” recovery. The “against all odds”, the “everything was against them”… the full recovery of a child who has had a terrible insult. The drowning, the fall, the pedestrian, the horse riding accident… all the terrible insults we see and all those mechanisms of injury that can potentially cause an early cardiac arrest or a moribund child.

Instantly we think of our algorithms, our protocols, our list of reversible causes and the sequence of steps we might take when we arrive at the scene. We hear the age, we think about weights, sizes, drug calculations. None of this should ever change and I’m not suggesting it should.

But what about when we hit that turning point?

It may have been an inkling early on. The thought that the mechanism is just too great, the injury just too severe, a poor response to even the most efficiently and expertly performed algorithm. It’s a moment where, sometimes even without verbalizing, the whole team is aware of the magnitude of the odds against this little one.

The Pause

What if in these cases we took a moment? Just a brief moment. When it comes to adult resuscitations I find we seem to automatically provide explanations to the family even while we are working. To explain that his heart is not beating and that we are working very hard to restart it; with a breathing tube, trying to stop the bleeding and with powerful medicines.

Perhaps it feels automatic because we just see more of those cases. We get to drill those algorithms more so there is a window that gives us space to look around.

So how do we provide this window in those paediatric prehospital jobs?

What if it was just a kiss before the transport? What if the family could have a little more from us? What if we suggested getting their daughter’s favourite teddy or blanket from the house? Just to fill their arms for the trip to hospital, to stop Mum’s hands from relentlessly wringing or something to give her tears a soft landing when they fall.

What do the books say?

The evidence for family presence during resuscitation has evolved over many years. Factors examined include the resuscitation team performance, stress levels amongst staff, clinical outcomes and psychological outcomes for family members. The evidence in paediatrics, including in some randomized control trials, demonstrates that there are improved measures of coping and positive emotional outcomes among families (1). These outcomes are achieved without impeding team performance.

There are many barriers to family presence in the pre-hospital arena. These scenes can be highly distressing, emotions are raw and the procedures required are time critical. Transport logistics can be a huge barrier too. It is rarely practical for a family member to travel with a child to hospital when they are critically unwell or in cardiac arrest. The confined environment of the back of an ambulance is usually congested and the potential unpredictability of a relative may compromise staff safety. The evidence regarding family presence is also more difficult to obtain.

I use this term in cases where I feel the resuscitation efforts are more a resuscitation for a family than the patient. I use it in the context of transporting to an appropriate place, where I feel that the optimal ongoing social supports for family members can be best met. Somewhere where others can assist with tissues, quiet rooms and hushed explanations. Somewhere where others can understand the welled up look that we give them when we enter the bay.

Now I think that the social resuscitation needs to start earlier. A more conscious and deliberate effort. Maybe not every time. Not when you can feel yourself buckling under the cognitive load. Not when your emotions are so close to the surface you can’t get the words out. Not when the scene is like a powder keg and you might just be putting people at risk.

But in those paediatrics cases we need to make a conscious effort to find a window, even where the algorithm is crowding us a little more. That might be the part of the resuscitation that isn’t futile for those left behind.

Try the explanation. Try the kiss. Wait for that teddy. Just try it and let’s see if it improves our social resuscitations. It might even just improve things for all of us.

Well everyone else is doing the “look back, look forward” thing, so why not us as well?

It’s that time of year. You know, the one where we just want a few more days to kick back and relax or enjoy a southern hemisphere summer. What better way to look busy than a review of the posts that got the hits in 2017? Ssshhh. There may well be better ways but this is what we’re going with.

First up, music for the ears

Podcasts. People do them and people listen to them. Clever people do them regularly. We are not that clever it seems. We did finally get around to putting up a couple this year though and the most recent one was very comfortably the most popular podcast we’ve done. OK, it’s a field of four but it’s not nothing.

The podcast features Dr Blair Munford. Blair has been in the retrieval and prehospital field since the mid ’80s. He has stories. Lots of stories. This story is his though and in it you get to hear a little about what it’s like on the day you’re getting picked up by the helicopter. So maybe have a listen. Lots of people obviously thought it was worth it.

The Not Very Final Countdown

We’re not packing up or anything so it’s nothing like a final countdown, but is there a theme amongst the posts that people seem to click on the most? Well let’s see. Here are the 10 top written posts through 2017:

The series on tactical medicine dates from 2016 but still gets plenty of interest. The third instalment just keeps clocking up the hits (and provides an easy link to chapters 1 and 2). People just want to know about phases of care I guess. If you like that you might also find this conference update worth your time too.

8. An old classic – little kid RSI

A couple in the year’s top 10 were all about kids which is a pretty pleasing thing. The care of kids isn’t just about shrinking stuff from adults and there’s plenty to gain from being kid friendly. This post went over the reasons that the approach to RSI in kids has changed and what we should be trying to focus on.

7. Necessity and the mother of invention

As much as we like kits sometimes you have to be flexible. This post on how to use what you have when you just have no choice is designed for when you’re stuck in one of those moments that will make you thank your gods for your real equipment when you’re back on a real job. Tourniquets? Check. Pelvic binding? Check.

This practical post on putting cannulas in little people certainly grabbed some interest. Maybe it will help out next time you’re facing a procedure that can cause pain at both ends of the needle.

3. More physiology when you pick a person up

This post comes from 2016 as well but it just keeps people coming up. A topic not covered that much elsewhere, but the physiology of a patient being winched is certainly relevant to lots of people in the rescue space.

We’ll level with you the rescuee here is apparently a mannequin so the physiology would be pretty forgiving but you get the idea.

2. In a bind

What is it about pelvic binders that gets people coming back for more. Our long running series on pelvic binders got a boost with number 5 which covered a case where the binder really probably didn’t help. You could drop by and end up down the rabbit hole of the other 4 posts with those links at the start of it.

1. Back to basics

And the top spot for 2017 goes to one of those great posts that covers things we often think of as basic but which might just make the biggest difference to patients – “basic” airways and adjuncts. Maybe you’d like to drop by this edition of those things we wish we’d known way back when we started.

So that’s the list. And the theme is pretty clear. People like practical things. And physiology. And things about kids. And things that touch on the literature. And … actually people probably just like all things prehospital and retrieval. Better get back to it.

First up is a big thank you to my co-author Pieter van den Berg from the Rotterdam School of Management in the Netherlands. Pieter is the real brain behind the study and the mathematician behind the advanced modelling techniques we utilised. Pieter has looked at HEMS base location optimisation previously in Norway and has done some modelling for Russel McDonald’s service Ornge in Ontario, Canada as well. Without him the study would not have been possible.

So what did we do and why?

As already noted Pieter had recently done a similar exercise in Norway where the government has a requirement that 90% of the population should be accessible by physician staffed ambulances within 45mins. Pieter and his co-authors were able to demonstrate that the network of 12 HEMS bases easily accomplishes this – indeed it could be done with just four optimally positioned bases. They also modelled adding and moving bases to determine if the coverage percentage could be optimised with some small adjustments.

As it happens New South Wales (NSW) and Norway have very similar population densities and both are developed, first world jurisdictions. Hence this previous study seemed a good place to start for a similar exercise in NSW. Both jurisdictions also have geographical challenges; Norway is long and thin with population concentrated at the southern end whereas NSW has almost all the population of the state along the eastern coastal fringe with high concentration along the Newcastle – Sydney – Wollongong axis.

We were interested in population coverage but we also wanted to look at response times as this also is a key performance indicator for EMS systems. It is certainly reported as a key indicator by NSW Ambulance. Response times were not modelled in the Norwegian system so we were interested in seeing how the optimum base locations varied depending on the question that was asked, particularly in a jurisdiction such as NSW where the population is so concentrated to a non-central part of the state.

If you look at the study you will note from Figure 1 the existing arrangements in NSW. You’ll be shocked to know these arrangements weren’t planned in advance with the aid of a Dutch maths guru. These things happen organically. Nevertheless it provides a reasonable balance of response times and coverage although the gap on the north coast is immediately evident.

If you start with a clean slate and optimally position bases for either population coverage or average response time, both models place bases to cover that part of the coast (see Figure 2). Hardly surprising. When we modelled to optimise the existing base structure by adding or moving one or two bases, the mid north coast was either first or second location chosen by either model too.

This seems an obvious outcome from even a glance at the population distribution and current coverage in Figure 1. What is surprising is that the 2012 review of the HEMS system in NSW (not publically released) which utilised the same census data in demand modelling did not come to the same conclusion when two previous reviews in the 1990s and 2000s had recommended just such a change. Certainly the Reform plan for helicopter services which was released the following year did not make any changes or additions to base locations leaving this significant gap still uncovered.

Wagga Wagga was the other location identified for a HEMS base in the 2004 review. Interestingly it is favoured as the first relocated base when the existing structure is optimised for average response time by moving Canberra to this location. But a Wagga Wagga base also was not mentioned in the reform plan.

What about the green fields?

When the green field modelling was done it is clear that the current NSW system mostly closely resembles the model optimised for average response time, rather than coverage. The Wollongong base really justifies its location on this basis as it contributes to a better overall average response time. Its population coverage falls entirely within the overlapping circles of the Sydney and Canberra bases so it makes no contribution here, at least if a 45min response time is used as the standard.

There was another aspect that interested us compared with Norway. In Norway all aircraft have the same capability and this is also true for the recently tendered services in NSW. The unusual feature in NSW though (unique to Australia although common in Europe in particular) is a dedicated urban prehospital service operating from a base near to the demographic centre of the largest population density – Sydney. The performance characteristics of this service have been well described (by us, because I’m talking about the CareFlight service which I think does serve a useful function) previously and when it was operating with its own dispatch system was the fastest service of its kind in the world to our knowledge.

Like the Wollongong service it operates entirely within the population coverage circles of other bases, but it makes an enormous contribution to average response time. When this rapid response urban service is added to the network of large multirole helicopters in NSW the average response time across the entire state falls by more than 3.5mins because that service is able to access more than 70% of the state population within its catchment zone, and significantly faster than the multirole machines.

This modelling only takes into account the response time benefit of the specialisation afforded by such as service. We have previously been able to demonstrate that the service is also much faster in almost every other aspect of care delivering patients to the major trauma services in Sydney only a few minutes slower than the road paramedic system but with much higher rates of intervention and ultimately passage through the ED to CT scan faster than either the road paramedic or multirole retrieval systems in NSW. At least this was the case when it had its own specialised dispatch system but that is a story we have discussed previously too.

There are recurrent themes here. The Rapid Response Helicopter service adds significantly to the response capability in NSW whether you model it using advanced mathematical techniques or whether look at the actual response data compared with the alternative models of care. Indeed the real data is much stronger than the modelling. It seems that at least in large population centres in Australia there is a role for European style HEMS in parallel with the more traditional multirole Australian HEMS models that service the great distances of rural and remote Australia. Different options can work alongside one another to strengthen the whole system and better deliver stuff that is good for patients – timely responses when they really need them. The capability differences however need to be reflected in dispatch systems that maximise the benefits which come with specialisation rather than a one size fits all tasking model that takes no account of those significant differences.

Every version of the numbers I look at tell the same story.

Notes and References:

While this post covers a few ways of looking at a tricky sort of problem, there are lots of clever people out there with insights into how these things work. If you have ideas or examples from your own area, drop into the comments and help people learn.

You might recall a series more than a bit ago from Dr Alan Garner covering lots of thoughts on pelvic fractures and what might make sense for prehospital care. Well, he’s back at it with a case to get things rolling.

It is amazing what you find when you go looking.

Those who are regular readers of the CareFlight Collective will be aware of my concerns about the use of pelvic binders in lateral compression (LC) type fractures. You can find parts 1, 2, 3 and 4 here. In short a binder in the context of a LC fracture replicates the force vector that caused the injury and may make fracture displacement worse. There is evidence of this in both cadaver models and in real live trauma patients. However blind use of binders without knowing the fracture type (and even where it is known to be LC) has been considered safe as there were no reports that patients had deteriorated after application – until now.

Last year one of our teams applied a binder to a haemodynamically stable patient with a LC fracture. There was immediate haemodynamic deterioration and new leg length discrepancy which had not been present prior to application of the binder. The case report has been accepted for publication by the Air Medical Journal and about now would be a good time to say thanks to our co-authors from Westmead Hospital, Jeremy Hsu and Anne Douglas. You can find a copy of the accepted manuscript accepted manuscript here. You need to go and have a read of the manuscript then come back for the following comments to make sense so I suggest you do that now.

Go on…

I can wait …

Continuing…

Now that you have read the case report you can appreciate that this incident caused us considerable angst. We knew this was theoretically possible but it was still a shock when it actually happened. It has caused us to review our practice around binders to try and find the safest approach.

But at the same time we need to acknowledge that we live in a space of considerable uncertainty because we don’t have radiographs to guide our management in prehospital care. All we have is our reading of the mechanism (which is often pretty unclear), the clinical state of the patient and perhaps a finding of pubic symphysis diastasis on ultrasound to guide us. We have to acknowledge that we are going to get this wrong a reasonable proportion of the time.

So here is our reasoning and the place we ended up.

Firstly we need to remember that there is still no study of any kind (RCT or cohort) that has shown a statistically significant improvement in survival with binders. There is some suggestive case series data (mostly in anterior compression or “open book” fracture types) and the benefit observed is raised BP and possibly blood product usage, not survival. That is it. As it seems we can definitely cause harm, it is worth keeping in mind just how poor the evidence for benefit is as we work our way through the approach to binder application. One of my very experienced colleagues refers to binders as “pelvic warmers” due to the almost complete lack of evidence of benefit and I can’t tell him he is wrong.

First…

The first thing to consider is the stability of the patient. Placing binders in stable patients with a possible mechanism has been considered acceptable practice despite the theoretical risks and indeed it is the policy of our local Ambulance service in NSW to do exactly that.

Other services such as Queensland have a more conservative approach. They position the binder if there is a suggestive mechanism but only tighten it if the patient is unstable or becomes so. Given that there is absolutely zero evidence that haemorrhage has ever been prevented by placing a binder I think the Queensland approach is a good one. I know that there are reports of binders reducing fractures so perfectly that they have been hard to identify on subsequent imaging and it is impossible to say whether they would have bled without the binder, but benefit from prophylactic use has not even been investigated let alone proven. And since we have now demonstrated that you can take a stable patient and turn them into an unstable one the summary of the published evidence now is:

Harm from binder application in stable patients = 1

Benefit from binder application in stable patients = 0

I acknowledge that prevention of haemorrhage is fundamentally difficult to prove but we have decided to join the Queenslanders. We will position it in stable patients if we are suspicious but it is only tightened if and when the patient becomes unstable. First do no harm. If they are haemodynamically stable you can’t make things better, but you can makes things a whole lot worse.

Second…

Our next consideration as per the previous posts parts 1-4 is the mechanism. If it is clearly a lateral compression fracture then there is not even a biologically plausible way a binder can help. If you are doing an interfacility transfer, you have an Xray and it is a LC fracture, do not apply a binder no matter how haemodynamically unstable the patient is. Every reported case who has had a rise in BP associated with a binder has had either anteroposterior compression (the majority of cases) or a vertical shear injury. Therefore the evidence base for lateral compression fracture so far is:

Harm from binder application in patients with LC injury = 1

Benefit from binder application in patients with LC injury = 0.

Just don’t do it.

Now of course prehospital it can be really hard to know what the fracture type is. But there are occasions where it can only be a lateral compression such as in MVAs where the impact is directly into the patient’s door with intrusion against their pelvis laterally. Here is an example repeated from part 3:

In this case the car has slid into the pole sideways. The impact is directly into the driver’s door who has been pushed across the cabin partially onto the passenger seat breaking the centre console in the process. This can only be a lateral compression fracture and that is indeed what was found on pelvic plain film in the ED. We no longer put binders on these patients, no matter how unstable they are – the binder has no plausible mechanism by which it can improve things.

Third…

The last part of the equation for us was the policy of application by the local Ambulance service which I have already mentioned. We often turn up to find that a binder has already been applied. Should we take it off again if stable? If unstable and it really looks like a lateral compression injury? The damage if any has probably already been done. We are operating in an evidence free zone here of course. Our consensus of opinion was that if it was properly applied we should just leave it there.

So we derived an algorithm which works through these steps in the reverse order that I have discussed them as that is the workflow in the real world:

So the only patients who get a binder placed and tightened are the unstable patients where lateral compression is not likely from what we can see of the mechanism or we just don’t know the mechanism. If you re-read part 3 this is the group we are suggesting that ultrasound may help in the decision making. Benefit (in terms of improved BP, not survival) has only been demonstrated in patients with a widened symphysis so perhaps this is your single best clue that you have identified a patient who is likely to benefit from the intervention – if such a group actually exists.

The Wrap

The belief that pelvic binders are a benign intervention is becoming widespread even though there are already reports of serious complications such as massive necrosis from pressure injury (have a look here). No intervention helps all patients, and all interventions carry risk. The key is identifying the patients where the benefit outweighs the risk. Given that proof of benefit from binders does not yet exist, think very carefully about the risk that you could make things worse by tightening it and converting a stable patient into an unstable one. Use it only where the possibility of benefit outweighs the risk and there is just no possibility of benefit in a known lateral compression injury. It can therefore never be justified if you know that is the injury type. Similarly there is zero evidence of any kind for prophylactic use in stable patients, just a theory and even the theory does not make sense in lateral compression.

I find it difficult to believe that this is the first time a patient has deteriorated with a binder – we are just the first group to report it because we have been looking. Complications are typically poorly reported in prehospital care for a number of cultural reasons (see Davis’ classic work on prehospital intubation where significant complications were picked up only by examining the monitor output; it was not reported by the clinicians). Perhaps the temporal relationship between the binder and deterioration is not as clear as in this case, or the patient is already unstable and it is not possible to differentiate the additional bleeding caused by the binder from the bleeding that was already happening. Or the subsequent instability is not attributed to the binder by the caregivers who think “just as well we put the binder on” without realising they actually caused it.

We would be really interested to hear if anyone else has observed this too. But you won’t notice if you don’t look. In the meantime I think we all need to examine our practices to ensure that are only applying the devices where there is a possibility that the patient will benefit from this as yet unproven intervention. If there is no possibility of benefit, just don’t do it.

Notes:

You could always start with public cases like this to reflect on what we could do differently with pelvic binders.

So you’re out there somewhere and you really want to do a thing you think might help but you don’t have your standard kit. Can you adopt the lessons of Richard Dean Anderson and improvise? Mel Brown has you covered.

Okay, so I am guessing from the title of this post you have a good idea of my age….I am talking about the original MacGyver, not the new one. And for those of you that are too young to know who I am talking about…..MacGyver could improvise everything he ever needed from anything that was “just” lying around. I once saw him create an explosive device with little more than a pepper shaker and some foil wrapping off some chewing gum.

It is wonderful that we live in a world where most of the time we have access to all we need (and more), including our medical equipment. But what happens when you don’t have what you need (or don’t have enough of what you need) to treat your patient?

So in line with our series on “I wish I knew then what I know now” we are going to look at MacGyvering (improvising) arterial tourniquets and pelvic binders – two devices that we are all very familiar with (or if you’re not you can be if you go …

These easily reproducible techniques are certainly something I wish I knew about when I first started nursing…..and no, it wasn’t when Florence was around (although I am pretty sure she trained one of my lecturers).

Continuing with the History Theme

Did you know that arterial tourniquets have been around for a while now? In fact, the first combat commander to advocate the use of tourniquets was Alexander the Great – he based his decisions on the works of the medical researches at Cos.

However it wasn’t until 1718 that Louis Petit, a French Surgeon, developed a “screw device” that could be placed over blood vessels to stop flow. From the French verb “tourner” (to turn), he named the device “tourniquet.”

Elegant, non?

Improvised Arterial Tourniquets

One of the most important things to remember with any arterial tourniquet is that indirect pressure MUST be applied whilst the tourniquet is being applied. This will at least minimise if not stop the bleeding whilst the tourniquet is being applied…

Improvised tourniquets need to be at least 5cm wide to ensure adequate arterial occlusion can be achieved. Have you ever wondered why a shark attack victim that has had an improvised tourniquet applied to their bitten leg (usually via a surfboard leg rope) soon begins bleeding again after the bleeding was originally stopped? Well the theory goes that the initial narrow occlusion of the artery was enough to completely occlude the artery but as the pressure proximal to the point of occlusion builds up behind the narrow improvised tourniquet the arterial pressure is able to beat the tourniquet and the patient begins bleeding again. You need something applied over a wide area to get the job done.

So, what should we use? Firstly you need to find a windlass device that is thick enough and tough enough to withstand the pressure applied to it as you twist it to tighten the tourniquet (which can be up to 300mmHg of pressure). Some things (and only some, there would be more) that are readily available include:

A thick solid stick (not always ideal)

An indicator lever (probably not out of your own car)

A screwdriver

A tyre lever

A set of pliers

As for the tourniquet itself, what should be used? Some materials used with good effect include (but again are not limited to):

Triangular bandages (make sure these are the cotton ones and not the cheap paper ones)

Seatbelts (once again probably not out of your own car)

Canvas belts

Shirt sleeve (preferably with non-stretchy material)

Neck ties (not sure how many of these are around these days).

One of the issues with improvised tourniquets is the narrowing of the tourniquet at the windlass point. This can pinch the patient’s skin and make an already painful intervention more painful. The narrowing of the tourniquet material can also lead to greater damage to the underlying skin, muscles and nerves. Having said that I am not sure the alternative of death due to blood loss is ideal either.

I think many of us have spoken about how we could improvise an arterial tourniquet….but how do we actually do it? Let’s use the triangular bandage as our improvised tourniquet to discuss this in detail.

Ideally you want two triangular bandages – lay the first one along the arm or leg.

Wrap the second triangular bandage over the first and around the arm or leg and tie a knot or two.

Place the improvised windlass rod on top of the knot and tie two more knots to secure that windlass (note: if you can’t tie knots, tie lots).

Turn the windlass until the bleeding stops and then turn once more. Secure the windlass in place with the first triangular bandage.

If you forgot the first triangular bandage you can use gaffer tape (or equivalent) to secure the windlass in place.

It is important to still write “T” and the time of application somewhere obvious (maybe on the patient’s forehead would catch the eye) as you would for any arterial tourniquet. Obviously improvising is not ideal when compared to commercially available products. However, they are life saving for your patient when you don’t have the equipment that you need available.

Improvised Pelvic Binding

Improvised pelvic binding has been widely used throughout Australia by our Ambulance services for a very long time – I think most people would be familiar with pelvic sheeting. There’s some nuance around when pelvic binding may or may not be useful (just check out the posts here, here, here and here) but what do you do if you’ve made an assessment it is worth trying and you’re without your fancy gear?

Well we all go driving or hiking with sheets in our car boot (that’d be a trunk for our North American friends) or backpacks, right? I don’t think so, and I know I certainly don’t. So what do we commonly have on us that we could use? A jacket works well as an improvised pelvic binder. Let’s have a look at what this looks like:

Prepare the jacket for use. Use the arms as a width guide and fold it up like so.

Place the jacket under the smalls of the knees where there is a natural hollow.

Preferably with two operators seesaw the jacket up to the correct position over the greater trochanters.

Bring the arms of the jacket together and tie a knot.

Twist those sleeves until the required pressure is achieved.

Secure that knot (gaffer tape works again, or zip ties or equivalent).

You’re done. And maybe cold, but done.

Once again it is obvious that improvising is not ideal when compared to commercially available pelvic binders. However they are life saving for your patient when you don’t have the equipment that you need available. All interventions, whether improvised or not, must be continually checked for effectiveness – especially if your patient is moved.

Summary

It is important that as clinicians we understand how to use the commercially made equipment we have available to us. However, it is just as important that we know how to improvise life saving interventions as there will be a time when we won’t have our equipment (or enough of it) to treat our patients. This is a predicament that I certainly don’t want to find myself in. So let’s share what we know as shared knowledge is power. Or share what MacGyver knows because that is also power.

Sometimes it’s worth wondering if the things we hear, see and feel are quite as we thought they were. Dr Alan Garner has a look at your senses when you get into the chest and wonders whether it’s all as straight forward as we like to think?

Let’s start this post by stating right upfront that this is about chest wounds. If that is not what you were thinking then time to look elsewhere.

What I want to discuss is the clinical diagnosis of tension pneumothorax in the field. The reason for the discussion is that I believe it is way over-diagnosed. When I worked in the UK 6 years ago it seemed tension was being diagnosed frequently and the reason given was the sound as they breached the pleura with the forceps. As the patient was positive pressure ventilated at the time then the sound must have been air rushing out of the pleural space as their intrathoracic pressure was positive throughout the respiratory cycle right?

Remember how we can’t rely on the sounds involved in clinical examination in the prehospital environment because they’re too unreliable? Well I was being told this one was always right. ‘Always’ is a big word in medicine

I’m also aware of at least one case where a patient with a single epigastric gunshot wound from a low velocity weapon had intubation and then bilateral finger thoracostomies. The comment at the time was that the prehospital doctor, who no doubt went into it all in good faith, stated that at the time of the thoracostomies they found a pneumothorax on one side and a tension on the other.

However on imaging and surgery the projectile went straight back into the pancreas and nowhere near either hemithorax or the diaphragm. Indeed the only injuries identified to any part of the chest were the thoracostomy wounds themselves. Again an intubated patient so the intrathoracic pressure must have been positive right? If the lung felt down then it had to be a pneumothorax? And if there was a sound on breaching pleura it must have been a tension?

Clearly in the second case the signs were misleading so what is happening here? Let’s put aside for a second the challenges of the initial diagnosis of pneumothorax and focus on the feel with the finger and the sound to the ears. Could it be that some of the evidence we’ve been lead to believe tells us we’re dealing with a pneumothorax can mislead experienced, well trained clinicians?

Diving In

Perhaps I have done a few more chest drains than most. Partly that is due to more than 20 years in the prehospital space but I probably did even more when I was a registrar 25 year ago. I spent 6 months working for a couple of respiratory physicians and I put lots of drains (mainly for malignant effusions) in patients who certainly did not have a pneumothorax before I started. It was common to hear a noise as the pleura was breached as the air rushed in. But this of course was in spontaneously ventilating patients and that is different right?

Obviously we need to go back to the physiology to see what is driving the movement of air either into or out of the hole we have made to determine whether the sound we are hearing is air going in, or air going out.

(If you’d like a little more on this the excellent Life in the Fast Lane has a bit on transpulmonary pressure here.)

Also it turns out that you can get a google preview of John West’s classic textbook on respiratory physiology. Take a moment to go and enjoy Figure 4-9 on page 59.

You can see from panel B (I meant it, go and have a look) that intrapleural pressure varies between about -5 and -8 cmH2O at the mid-lung level during normal respiration. It is always negative and that’s due to elastic recoil of the lung which is being opposed by the chest wall. It is less negative at the dependent regions of the lung (reducing alveolar size) and more negative at the apex (increasing alveolar size).

Let’s Add Air

In the situation of a small pneumothorax the air in the pleural space makes the intrapleural pressure less negative and the driving pressure difference for ventilation is therefore reduced. If the pneumothorax is completely open to the air such as with an open thoracostomy wound the intrapleural pressure is equal to atmospheric pressure, the elastic recoil of the lung causes complete collapse and ventilation by chest expansion is impossible – positive airway pressure has to be applied.

It is not the situation of the pneumothorax that particularly concerns me. If they are hypoxic or hypotensive and the patient has a pneumothorax the chest should be decompressed – a complete no-brainer. The question is why are good clinicians decompressing normal chests and thinking there was a pneumothorax or even a tension when there was not? Does the physiology lead us there?

Patient One

First let’s consider the non-intubated patient with normal respiration and no pneumothorax. This is the situation with the patients with malignant effusions I was putting drains in years ago. Here the alveolar pressure is never more than a cmH2O or two positive or negative. The intrapleural pressure however is -5 to -8 cmH2O. Therefore it does not matter what phase of respiration you breach the pleura, the pressure gradient between the pleural space and atmosphere is negative and air will rush in.

The gradient is bigger in inspiration when alveolar pressure is negative (and therefore the total pressure is around -8 cmH2O) and less negative during expiration when it is more like -5 cmH2O. It is however always negative. It does not matter which part of the respiratory cycle you breach the pleura, air is going to flow into the pleural space and the elastic recoil of the lung will drive it to collapse. If you hear a noise as I often did, it is air rushing in, the classic sucking chest wound. An iatrogenic one.

Patient Two

I don’t think anyone would have an issue with things so far. So let’s move on to the intubated patient who does not have a pneumothorax. I am going to assume here that there is not a lot of airway resistance in our trauma patient (which is not to say they don’t have underlying obstructive pulmonary disease, anaphylaxis to the induction drugs you gave or a clot sitting in a big bronchus/ETT) as it makes the discussion a bit easier to assume that resistance is minimal (futile according to the Daleks) and the pressure you are seeing on your ventilator gauge is largely transmitted directly to the alveoli.

Looking at our transpulmonary pressure equation, unless the airway pressure and hence alveolar pressure is higher than about 5 cmH2O then the gradient at the time you open the pleura means air is going to enter the pleural cavity. (If they have significant airway resistance this could happen with much higher airway pressures).

Just have a quick eyeball of this time pressure chart of a standard volume cycled ventilator with no PEEP (and a self-inflating bag will provide a similar though more variable trace). And I deliberately have no PEEP in this chart. PEEP is not likely to be the first thing we reach for in the hypotensive trauma patient we have just intubated where we are concerned about the possibility of a pneumothorax.

With normal lungs the peak pressure here is probably about 20 cmH2O. What proportion of the total respiratory cycle is the airway pressure (and hence the alveolar pressure in our patient with low airway resistance) likely to be below 5 cmH2O? If your little prehospital ventilator has a roughly 1:2 I:E ratio as most do, then the answer is most of it.

In other words unless you have PEEP of at least 5 cmH2O even in your intubated patient the transpulmonary pressure is negative for a good half of the respiratory cycle. During at least half the respiratory cycle, if you hear a noise as you breach the pleura you are hearing air rushing IN.

The elastic recoil of the lung is the reason that you feel the lung has collapsed by the time you pull the forceps out and put your finger in unless you have some PEEP in play.

Now I’m not saying there has never been a time when the air wasn’t rushing in. I don’t think much of the word “always” in medicine, remember? I’m just suggesting that what we know of physiology would argue that there is at least a solid proportion of the time where that transpulmonary pressure gradient is negative when you breach the pleura, which means that there’s likely to be a good proportion of cases where those “certain” clinical signs become less reliable.

For a demonstration of this with the mother of all open thoracotomies (in a cadaver) check out this video.

The cadaver is intubated, a “generous” pleural decompression wound has been created, and on each expiration the lung collapses right down unless PEEP is applied. And note the collapse is complete on each expiration.

As long as the thoracostomy is big enough to freely communicate with the air (and if you are relying on the open “finger” technique rather than putting in a drain it needs to be large or they may re-tension), when you put your finger in during expiration the lung will be collapsed unless there is a reasonable amount of PEEP splinting things open pretty impressively.

It will be collapsed whether it already was before you made the wound or whether it happened as you spread the forceps and made the communicating hole. The time between making the hole and getting that sense of lung up or lung down with the finger is ample time for the lung to collapse down. It seems like this particular clinical sign probably tells you nothing about the state of play prior to the wound being made.

So noises can be deceptive and feeling a collapsed lung just means that the lung recoiled as the pleura was opened. Can you even guarantee which phase of the respiratory cycle the patient was in when you made that hole? Unless you had at least 5 cmH2O (and maybe more) PEEP on at the time you breached the pleura neither of these signs necessarily means anything.

Maybe none of us can trust our big ears?

Now, what?

Again, I’m not really into saying things like “always” or “never”. What I’m suggesting is that there might be a lot more grey around these clinical signs than might first seem to be the case.

So how do you know if they had a pneumothorax? For me that is almost always by ultrasound now. I don’t know how I managed for 15 of those 20+ years of prehospital care without one. Sometimes of course the scan is equivocal and you need to make a call based on the signs you see and the condition of the patient but I find this to be very infrequent with a good high frequency linear probe.

And as for tension the hallmark is abnormal physiology, particularly blood pressure. If decompressing the chest fixes the physiology then they had a tension. If it does not then they had a simple pneumothorax – or none at all. Because the noise you heard as you breached the pleura may have been air either entering or leaving the building, hearing a noise does not help you either way. Was Elvis ever in the building at all?

Notes:

I had the brilliant Dr Blair Munford review a heap of the physiology here to make sure it matched up.

After that link to the LITFL bit on transpulmonary pressure again? Then go right here.

And John West’s masterpiece (well at least the page mentioned) is here.

That image of Nahni with the big ears was posted to the Creative Commons part of flickr by Allan Henderson and is unaltered here.

Oh, and in case you didn’t know the truly amazing John West, Adelaide boy made good, has recorded his whole lecture series for you to go and watch. Because when you’re in your 80s you’ll probably be contributing to medical education like that too, right?

At the recent Student Paramedics Australasia International Conference 2016 held in Sydney, Dr Andrew Weatherall was given the topic of “things paramedics can do to produce better long-term outcomes after traumatic brain injury”. This is a version of that talk modified for the blog.

This topic, that someone else came up with, gets it.

So much of the time in prehospital medicine we focus on things we measure in the first hour or so. The stuff we do before we hit the doors of the hospital. That fairly bogus ‘golden hour’.

Those things matter. But the big picture of trauma care isn’t the first hour. It’s the rest of the patient’s life.

Everything we do in the prehospital setting is really about whether they get back to what they were dreaming of doing. It’s not up to us what those dreams are. Your patient might dream of playing big time sport. They might dream of creating the world’s great collection of corn chips that look like ex-Prime Ministers. They might want to fly on the first trip to Mars (and almost certainly die of cancer because everyone seems to be forgetting about deep space radiation). When we care for them we sort of have to want their dream to happen for them.

So on the days when I get to hang out with paramedics instead of getting paid by the government to wear pyjamas and give drugs to kids, this is the aim. And traumatic brain injury is worth looking after well.

We could dive into traumatic brain injury by starting with a bunch of graphs from a physiology text. Let’s dive into something to make it relevant.

The Scene

This is the scene we’ll be going to. You’ll end up looking mostly at the patient who was driving the SUV. It looks like they had an initial collision, rolled over and then nudged up against the hatch that was veering off the road. Emergency services have been called by a passing pharmacy student who has done a First Aid course. They tried shaking and shouting and got no response. They thought about feeling for a pulse and they’ve found one.

This patient is clearly one who might have a traumatic brain injury (TBI). They could end up as one of the patients with moderate or severe TBI who lead to a cost to the system of around $8.6 billion each year. That comes from a report prepared for the Victorian Neurotrauma Initiative released in 2009. It estimated that for 2008 Australia would have around 1400 in the moderate TBI group and 1000 in the severely injured group.

And each one of those people doesn’t get back to their planned life. Some of them end up needing help with simple things for their whole life.

So this is the job and the clock started 5 minutes ago. What should we focus on? Is it all about RSI? Is it about early TXA? Is about the sort of stuff you need an advanced medical team for?

Well that could be the basis of discussion but we should start with a reality check.

If you look at the NSW Institute of Trauma and Injury Management report of the 2014 trauma database stats, there were 3458 severely injured trauma patients. 66% of the patients had an injury to the head. 3 of the top 5 severe injuries were subdivisions of subdural haematomas.

Of those arriving straight to a trauma centre, 80.4% arrived in an ambulance (vs 12.6% in a helicopter).

Even allowing for some of those ambulances having an accompanying advanced prehospital team, I think this grouping of numbers says something pretty significant: the vast majority of “big” trauma patients will get their care from paramedics.

This also means that if we want to save the most brain cells we should focus on making sure the patients getting those transports have the best possible care that those paramedics’ training can make happen. That’s more important across the population than the advanced team’s contribution.

There is a separate chat to have some day about trying to get advanced teams to the jobs where they might really help or the best way to do pointy end stuff. That’s just not the focus for this particular bit.

It does brings us to the first key thing that trained paramedics can do to improve long-term neurological outcomes – be there.

The nature of their training and their ability to focus on getting the vital things done and get moving means that paramedics will invariably lift the standard of care of the patient when they turn up and do their job.

Now exactly what they should do we’ll get onto in a bit but there will only ever be a small number of meaningful interventions to do for the patient so it makes sense to get it done as efficiently as possible and get moving. And of course while neurosurgery is mostly not an urgent requirement, about 1 in 5 patients will need some form of early head-cutter work. That 20% of patients really want professionals who are trained to make things move.

So it might seem like there’s not much meat on just saying “be there”, but I think it’s worth noting as we go that the standard way professional paramedics go about their business represents a step up compared to what was managed in the past.

Now that you’re there …

Back to the patient. When you get there, the patient looks to be in their mid-30s, is making breathing efforts and there is some air moving but it is fairly noisy respiration. Initial peripheral saturations read at 85% and the measured blood pressure of 95 mmHg is somewhere near what you would have guessed by palpating the radial pulse. The patient’s GCS is 7, the pupils are equal and reactive. A quick glance suggests the right femur looks like it’s adopting a more meandering course than usual on the way down to the knee.

So what should our aim be for these patients? What targets do we have that are the best evidence-based ones available?

Somewhat disappointingly we don’t have that much evidence for discrete targets. What evidence there is hasn’t really shifted much over the last couple of decades. Most of the stuff we do leans heavily on a general understanding of physiology as much as firm numbers.

But let’s focus on the numbers we do have. They’re based mostly on retrospective looks at info from big data banks. And the number to remember is 90. That’s the breakpoint because:

90% saturations is around 60 mmHg pO2 and we know that patients who have a reading below that value have worse long-term neurological outcomes.

90 mmHg is the magic BP number for adults – a measurement below this is associated with worse outcomes.

And these markers kind of make sense. We often think about the primary injury already having happened when we get to the patient and focus on avoiding secondary injuries which we view as discrete and separate extra insults. Add new injuries and you make the outcome worse.

It’s probably more accurate to say that the primary injury evolves over a number of hours. In that traumatised brain there will be excitatory neurotransmitters looking to party way too much for the cells to recover. There will be inappropriate triggering of cell death. Calcium will be getting places it shouldn’t and generally grabbing onto cell elements it should leave alone. Each secondary injury ramps up processes like these as they continue to evolve. It’s one of those times all evidence-based practitioners need to try and stop evolution from being a thing.

There are a few other things worth keeping in mind:

The brain is pretty simple in its demands. It wants oxygen and nutrients delivered.

Things that make blood flow decrease aren’t good (remember that the injury itself is quite likely to drop blood flow well below normal).

Intracranial pressure that is high isn’t great. It compromises blood flow.

Oh, and it’s also worth mentioning that there aren’t many things inside the head that we influence the volume of prehospitally:

There’s the brain tissue (and the associated fluid that goes with it).

There’s blood. Blood can be inside vessels which gives us some scope to manipulate how much flow is occurring. Occasionally it will be outside vessels and the vast majority of times that patient will get their definitive care at the hands of a neurosurgeon.

There’s CSF (which we have less influence over).

So if our aims are basic do we have to wait for advanced techniques to try and reach this target? Of course not.

This brings us to the second important “thing that we can do right now” – be basic.

Consistent delivery of basic measures has the potential to save huge numbers of brain cells. It’s more meaningful than waiting to try and develop the infrastructure and expertise to get more people doing advanced things like RSI.

The perfect example is impact brain apnoea. This has really only been described in any detail fairly recently by Wilson et al but there are accounts throughout medical history and the animal literature that describes a phenomenon of subjects forgetting that whole breathing malarkey in the immediate aftermath of trauma.

The suggested treatment? Open the airway and support ventilation. Those simple steps are meaningful.

They’re meaningful for all patients with TBI too. Which is why it’s worth getting back to the simple message of “A-B-C” which some sage once told us was as easy as “1-2-3”. Simpler than the transition to adulthood from child stardom if you were that individual anyway.

So let’s work through those simple little letters.

1. How’s your “A” game?

Well, is it anarchy?

Failure to do the basic bit of airway well is one of the commonest issues we see when welcome people training at the kids’ hospital. It’s such an important foundation though. So ask yourself whether you do the basic version of “A” well. Is your jaw thrust good enough to get those bottom teeth in front of the top teeth? Do you reach for adjuncts like oropharyngeal or nasopharyngeal airways as an aid? Are you quick enough to move to a two hand technique?

Most importantly do you make sure that you create a good seal with your mask? The value of a good seal is actually highlighted by work looking at pre oxygenation techniques. A colleague from CareFlight, Dr Chris Groombridge, did a nifty study with volunteers evaluating the maximum expired oxygen level you could achieve with different techniques. Anaesthetic circuit vs bag-valve mask (either alone or with nasal cannulae or PEEP valve or both) vs non-rebreather mask (with and without nasal cannulae).

And at the end of 3 minutes you still couldn’t beat either the anaesthetic circuit or the bag-valve mask with a well-maintained seal.

Hayes-Bradley et al did some work with a slightly different focus, evaluating the impact of nasal cannulae on pre-oxygenation with a bag-valve mask set-up or non-rebreather. Nasal cannulae helped only where there was a deliberately created leak in the seal.

Now you could take the line that it’s just pragmatic to assume you’ll end up with a leak. But why should we accept doing the technique anyway other than perfectly? Let’s focus on getting the seal right.

We’ve really taken that to heart at work, making the effort to maintain that seal throughout pre-oxygenation. It’s all part of ensuring that our focus on is on the main game – maximising oxygenation throughout the RSI rather than pushing on to the laryngoscopy and intubation step without optimising things up front. The brain wants oxygen more than it wants laryngoscopy.

That some prioritisation of the basic step of managing “A” well – perfect performance of basic airway manoeuvres, suction and use of adjuncts – can apply to all of us, whether we intubate or not. It’s the first step to delivering on our first aim – get those peripheral saturations above 90.

It also feeds seamlessly onto …

“How good are your “B” moves?”

Is it carnival material?

What about those patients who need support for the breathing part of the equation. That might be via that bag-valve mask set-up or you might have supraglottic airways as an option you’ve been trained to use.

The question here is not just how well do you do it but do you take steps to make sure you’re using that skill set in the best interests of the patient?

So if you think a supraglottic airway might be appropriate for a patient do you quickly assess if they’re ready for it with a firm jaw thrust and a deep suction before placing it? Do you check what the seal is like once it’s in?

And how do you measure your effort with the bag you hook up to that SGA? Because it’s easy to puff away like your hand is a talking sock puppet. We should really all be hooking up capnography wherever we can (for bag-valve mask work too). It might not provide a trace like the intubated patient but it will be more accurate than a guesstimate. And without having a sense of where you’re at with the CO2, how do you know if you’re not creating hypocapnoea when hypocapnoea is associated with reduced cerebral blood flow (and of course hypercapnoea could cause raised ICP)?

Doing the “basics” well requires a bit of attention. Who knew?

But you might well say, what about RSI? Shouldn’t we be figuring out how to train people to do that? Well while there is a probable role for RSI it is really hard to demonstrate the positive benefit. That is probably partly because prospective research in prehospital medicine is very hard. But the evolution of the research that’s out there suggests that getting that high stakes procedure done well enough to have the benefit outweigh the potential complications will take a very long and concerted effort.

Take for example just 3 studies:

The San Diego RSI paper – this suggested worse outcomes but subsequent analysis revealed performance of the procedure with significant periods of hypoxia (57% of those analysed had a desaturation with an average time of 160 seconds and a median fall in saturations of 22%).

HIRT – which took long enough in recruitment that the system changed all around it, rendering it very difficult to keep arms of the study in their planned arms. Those that received the advanced interventions team as intended did have a 14% reduction in mortality but it’s not robust enough to bank your house on.

The Victorian paramedic RSI paper – this showed benefit but there were more patients in the control group lost to follow-up and you’d think that those who did better would be the ones you’d lose. Just one different outcome in the control group would have made the findings insignificant. So it’s not robust enough but for different reasons.

So RSI makes physiological sense and most would still say it has a role. But it’s hard to make it pay off. We can all do the basics right every day from today.

What should we see when people are doing “C”?

It’s not like there’s some study out there saying “this particular prehospital intervention related to circulation and haemorrhage leads to better TBI outcomes” but we can focus on maintaining that blood pressure above 90 mmHg. So things that cause catastrophic hypotension (say, pneumothorax with haemodynamic consequences) need treatment with whatever the provider is trained for.

If there is external haemorrhage that has to be controlled so we can focus on doing that particularly excellently. If you’re putting on a tourniquet, think about providing proximal occlusion of flow first with your whole weight (e.g. a knee not just into the groin but leaning in and twisting a bit to really slow down flow before the tourniquet goes on). Really provide pressure to stop bleeding if pressure is the treatment you’ve chosen. Splint that femoral fracture to reduce loss of blood volume.

At the same time it’s worth noting that some of the evidence base for things we do is less strong than we might assume. As covered by Dr Alan Garner in the series starting here, the evidence base for pelvic splints improving haemodynamics isn’t based on huge reams of work.

Other options will probably come through for lots of practitioners soon. Haemostatic dressings or granules are likely to make a difference for some patients. With a little more evidence TXA might roll out across the land. And while there are very interesting concepts like prehospital REBOA out there to be wielded by a select few, something like the Abdominal Aortic Junctional Tourniquet might be a far more significant option on a population level. Judicious use in the exsanguinating patient with due regard to the potential downsides (particularly if it might take a while to get to somewhere else) could be an option for an awful lot more practitioners.

The Other Simple Things

That’s not the end of the simple things of course. Think about whether you can sit your patient up to drop the ICP. Is there a better way to maintain C-spine stability then a rigid collar? Is there anything constricting the neck?

Add a lot of simple steps together and you have pretty comprehensive efforts for those brain cells that just want blood to flow and nutrients to turn up.

The Group Who Doesn’t Get the Simple Things

And while we’re at it, there is one group who tend to get much less of all of the things, including the basics.

Kids.

Which is not great if you’re trying to think about how to provide better long-term outcomes. Their long-term is even more long-term.

Bankole et al provide just one example of a study demonstrating this. They looked at prehospital care around a New Jersey centre and compared the care received by kids with TBI to that received by adults. The numbers are pretty stark (though some of the headline items relate to interventions like intubation).

69.2% of the kids intubated had complications at intubation. 20% of kids with a GCS under 8 had no attempt at intubation. Failed intubation rates were 29.03% (vs 2.27% in adults). Kids also had higher rates of the dislodgement, oesophageal intubation, wrong size of tube choice and a requirement for multiple attempts.

Even intravenous access was placed less (adults had a prehospital cannula 85.9% of the time whereas in kids with the same spectrum of pretty severe injuries it was 65.7%).

More recently advanced practitioners in Switzerland published around the topic of advanced airway management in kids and while they did well initially, wrong tube sizes and wrong depth of the tube turned up again.

There are lots of reasons we do less well with kids. We see them less for a start and there can be additional scene distractions. But ultimately we need to recognise this and figure out a way to make sure we step up to the mark.

Back to the Scene

The patient has been making respiratory efforts but you can see the chest see-sawing a bit with diaphragmatic effort with an added breathing buzzsaw soundtrack. You jaw thrust and the airway improves. A suction improves the airway still further. You add a bag-mask set-up and really focus on a great seal. The saturations rise above 95%. The femur looks like it’s taking a meandering the scenic route towards the knee but it’s soon splinted and a big wound in the calf gets pressure to slow the bleeding. You’re on your way…

Now that sounds pretty easy. When you’re in a lecture theatre or reading a lesser known blog it sounds even easier. But we all know that the scene isn’t actually that easy. We’re assailed by all sorts of things and there is plenty of work in simulation sessions (like here) showing that when faced with high stress situations we tend to omit things we ordinarily wouldn’t, do things we’d normally not contemplate and remember all of it less.

This touches on the next thing prehospital practitioners have to do to provide better care for the brain – be the same with your care, everywhere. (The astute reader will notice that not only did I match the formatting to the other “be” statements, I made it internally rhyme. I’m really trying to make it seem meaningful.)

Beyond starting by acknowledging the risks of a deterioration in performance depending on the day or the job or the other stuff in our lives, we have to figure out how to be consistently excellent with our care. That’s what the patient expects. Their brain cells aren’t very interested in your back story or your motivation. They’d like you to do your job.

The strategies to try and make sure you always step up are way too many to go in right here, so it’s worth looking around. But use the team, communicate well, share your plans with those around you, use checklists or practice tactical breathing or other focus techniques or whatever it is that works for your good self.

Just don’t accept that you have to be a hostage to all those other factors.

And part of not accepting the status quo is striving to always provide better than we can do right now. That requires all of us to be a leader.

If we want to be able to provide capnography for all those patients whose A and B we’re managing then we might need to advocate for that. If we want to be able to look back in detail at how well we did, then monitors that only store information every 2 minutes (which is so often the case with prehospital monitors) aren’t up to scratch and we need to lead those demands. We need to provide leadership in governance and education to keep our standards constantly improving. We might even need to advocate solutions to issues in other areas of health that would free up paramedics to be out on the roads so they can work on that being there bit.

Future Dreams

While this topic is mostly about what we can do right now we obviously have to keep an eye out for what comes next. And I could well be wrong but my guess is that the thing that comes next that makes a big difference across the population to those who suffer a TBI won’t be one of the magic bullets being tried like progesterone, or EPO, or even TXA.

What would be really great is to actually know what the brain wants right now. Is the blood pressure of 100 mmHg actually adequate for this person’s brain or are they usually hypertensive and critical cerebral ischaemia is being added to your mix?

Does this patient actually need their CO2 a little higher than you might have thought because blood flow isn’t so great? Is their evidence of haematoma developing on one side that hasn’t shown up clinically?

That’s part of why we’re researching tech like near-infrared spectroscopy tissue oximetry. Now I’m not convinced that particular technology will provide that information reliably enough, but I do think that the most meaningful thing we could add to prehospital TBI care is more info about what this patient’s individual brain would like, rather than being stuck with population-based gross numbers.

And if we find that device the ultimate result will probably be that it tells us how to do the basics just that little bit better for this particular patient.

Because they might have big plans for corn chips that look like ex-Prime Ministers.

Notes:

OK, this was a really long post, but when you put a talk into post form it can be like that.

Here are just a few things from along the way you might like to go and look at.

Oh, and I put stuff over on the blog site at www.songsorstories.com relating to kids anaesthesia. If you look at the categories “airway” and “tips and tricks” and “cannulation” you’ll find some basic tips for working on things.

Dr Alan Garner has a blog post in the context of a report just published. A catastrophe during a winching operation highlights the physiological challenges we sometimes add in the work we do.

The death of a patient during a winching incident in Victoria in 2013 was distressing for everyone concerned. I was asked by the Victorian Coroner’s Office to provide an expert opinion on the death based on some previous research I had conducted with one of our registrars, Dave Murphy, looking at the effects on respiratory function of various methods of helicopter rescue. I’m pretty sure at the time we were the only group in Australia who had published in this area so I guess we were the obvious choice.

As part of trying to avoid a similar incident the coroner’s office agreed to us publishing the case in an appropriate scientific journal so that operators worldwide would benefit from the lessons learned rather than just the industry in Australia. That report has just been published in Aerospace Medicine and Human Performance and can be found here.

The details of the case are now on the public record in both the coronial inquest and the ATSB investigation. Our case report focuses more on the physiology of hoisting than either of these forums needed.

For those not aware of the case the brief version is that a man of approximately 60 years of age and BMI of 45 with borderline cardiac failure injured his ankle whilst on a hunting trip in Victoria about a kilometre from the nearest road. Carrying him was considered risky for the rescuers (the terrain was steep) and a hoist extrication by helicopter was organised. An accompanied single sling technique was utilised.

Unfortunately as they approached the aircraft skid the patient became combative and then unconscious. He slipped from the strop despite the best efforts of the paramedic and crewman and fell to his death. I can only imagine the distress of the crew when this occurred.

The actions of the crew on the day were consistent with their company/Ambulance Victoria procedures and were within the specifications of the equipment utilised. They were just doing their best to provide their best care as they’d been trained. Neither was any of the equipment found to be faulty. The obvious question then is why did the fall happen?

What happens when you put someone in that hoist?

You need to go looking in the climbing literature to find the physiological effects of suspension with chest compression which is what happens when you are in a single strop. As you would expect, there is a constrictive effect upon respiration but there is also a considerable decrease in cardiac output resulting from the decreased venous return with raised intrathoracic pressure. The decrease in cardiac output has been demonstrated to be as much as a third in fit young climbers. The decrease in respiratory function parameters is similar (in both the Murphy paper and the one referenced in the link in the previous sentence).

When you think through what’s involved, the physiology makes sense.

Given that the chest compression associated with hoist rescue is of short duration it is generally adequately tolerated long enough to complete the rescue in fit young people. Having said that one of the best studies of the physiological effects of suspension in a chest harness was precipitated by the death of a 25 year old soldier who was left suspended in a single strop for just 6 minutes. Cardiovascular collapse can occur surprisingly rapidly. The man in the Victorian incident with his significant comorbidities was however not able to tolerate even a short period of thoracic compression and rapidly became unconscious.

The effects of single strop rescue in people who have been immersed even where they are otherwise fit and young is perhaps better known and the second sling under the knees (or hypostrop as it is often called) is in widespread use in this situation. For winches of non-immersed persons it seems that the physiological consequences of various rescue techniques are not well known in the industry however.

Subsequent actions by Ambulance Victoria, the helicopter operator, the Victorian Coroner, CASA and the Australian Transportation Safety Bureau (ATSB) all rightly concentrated on determining how a repeat of the incident could be avoided by better educating both clinical and operational crews about the physiological implications of hoisting techniques.

What are the options?

We have previously published on the use of the Coast Guard Rescue Basket due to its benign effect on physiology compared with other techniques (Murphy). It remains a surprise to us that this device is not in more widespread use. Ambulance Victoria has now introduced a sit type harness which is definitely to be preferred in hoists over land. The Rescue Basket can be used in winches out of water as well and we think is the more flexible option.

You can see that this sort of option would be easier on the physiology.

Should the single strop technique be banned entirely? We don’t believe so. Every rescue is a balance of risks and sometimes the risk to either the patient, aircraft or both means that an immediate single sling extrication may be the safest option overall. We certainly have not banned its use within CareFlight. Knowing about the physiological downsides we have discouraged its use for many years and encouraged use of the rescue basket. We have not removed it from the armamentarium however. If a crew elect to use it they have to provide a report in writing to the chief pilot about why they chose that technique. Knowing that there is that little bit of extra documentation required is enough to make teams make sure they’ve covered their options and risks carefully before they go ahead, but the option remains on the table.

Hoisting is risky for lots of reasons. We train for a range of safety considerations. And equally we have to make sure we’re aware of the physiological changes we might inflict on our all important patients.

Conflict of Interest Statement:

Neither I, nor either of my employers have any interest, financial or otherwise, in the manufacturer or distribution of the Coast Guard Rescue Basket.

Continuing the series of sharing Carebundles, Alan Garner moves on to go through the stuff to include in multiple blunt trauma.

OK, part 2 in our Carebundle series. This time we will take a look at our multiple blunt trauma bundle. This excludes isolated head injury which we dealt with in the previous post. Why that order you may ask? Our Sydney service started life as a trial evaluating the management of severe head injury so TBI is front if mind for us. It is also more straightforward as there are not the competing priorities that occur in multiple trauma. And in the end we don’t just want survivors but neurologically intact survivors so starting with TBI and brain resuscitation makes sense. The multiple blunt trauma bundle has conditional targets that are modified by the presence or absence of brain injury acknowledging that brain resuscitation is our major goal.

So multiple blunt trauma is next. This has many bits of intrigue to it. It is multiple. We’re moving into the bits of the body where the pathology can be buried in the large splodgy bit in the middle. The diagnostic stuff can be pretty challenging at the side of the road. Oh, and because it’s multiple there’s always that threat of a new competitor emerging in the pathophysiology parade.

We won’t touch on penetrating trauma, burns and immersion all of which have their own bundles of joy for another time.

The Common Touch

All of the mandatory items overlap with the TBI bundle so we won’t waste any time on them here:

Venous access – yes we reckon that still makes sense.

Analgesia – opioids/ketamine – yes we’re really trying to stress that analgesia is a vital component of care, pretty much every time.

Monitoring: SpO2, NIBP, ECG

Spine immobilisation – note we’re just sticking with immobilisation.

SpO2 > 93% by ED arrival

Scene time < 25 min – again, this isn’t always possible which is part of why Carebundles provide guidance but need clinician judgment on each job. What we’re aiming for is a background enthusiasm for keeping momentum throughout the time we’re looking after patients so we can get them to the hospital with all those eager people waiting.

Transport direct to trauma centre – this would be the house for the eager people.

The conditional items however vary from the TBI bundle and we will now go through these.

Checking the Terms and Conditions

Long bone fractures splinted

There is no evidence I am aware of that this changes outcome but it is standard ATLS teaching and makes pain control easier. We carry lots of excellent drugs and the Carebundle makes a point of mentioning them but everything is easier if you manage the physical elements contributing to the painful situation. Really this is the original multimodal analgesia. It’s just that one of the modes is “physical things that stop hurting things from exercising a right to freedom of movement”.

Massive external haemorrhage controlled

There is strong cohort level data that this saves lives, although more so in the penetrating trauma context where it is more common. Certainly data from recent conflicts supports this as a primary aim of prehospital care. So we’re carrying tourniquets, dressings, chitosan gauze and granules (though the latter are more for penetrating wounds).

Right here seems to be a point to salute the wondrous quality of the shells of prawns.

TXA if episode of SBP < 90mmHg, or below normal for age

CRASH 2 inclusion criteria were felt to be a little vague to include in our bundle. After all the inclusion criteria in this study was any trauma patient who was at risk of haemorrhage. To make the bundle we felt the item needed to identify the cases where TXA really should have been given because the risk of life threatening haemorrhage is so high. There is some evidence that just a single episode of documented hypotension is enough to identify a group of very high risk patients so we adopted this as our criteria. As another mental trigger point, some of our team have expressed a process when they consider packed cell transfusion – “If I’m reaching for blood, I should reach for that drug.”

If shocked, SBP at ED arrival (refer fluid guideline)

No head injury: palpable central pulses/obeying command

With head injury: Palpable peripheral pulses, or SBP > 90mmHg / lower limit of normal for age

In setting our blood pressure targets we differentiated between those with and without head injuries. Without a head injury permissive hypotension is our strategy. With a head injury we adopted the lowest level identified in the Brain Trauma Foundation Guidelines i.e. SBP of 90mmHg as our target. This is lower than our target for isolated severe TBI where our target is a MAP of 90mmHg or SBP of 110mmHg (see the TBI bundle post for further details). That last modification is obviously for paediatric patients where the guidelines are a little harder to attach specific numbers to.

If GCS < 9:

Intubation and mechanical ventilation

EAM above JVP (head elevation)

ETCO2:

30-35mmHg if no chest trauma/shock

25-30mmHg if chest trauma/shock present

This is similar to our isolated severe TBI bundle but we finesse our etCO2 targets in the presence of other injuries that might affect the gradient between arterial and alveolar levels. There is some evidence that adopting a lower prehospital etCO2 target in patients with chest trauma and/or shock is reasonable as these patients have predictably higher gradients. My own personal experience is that in patients who have both chest trauma and shock the target needs to be even lower. I have achieved an etCO2 by ED arrival in the mid-twenties in patients where both these factors are present only to find the first blood gas reveals an arterial level in the 50s. I would certainly be interested in hearing other people’s experience on this one. Of course in our rapid response urban trauma work we don’t carry a POC blood gas analyser like we do in our interfacility transport operations. Actually measuring the arterial CO2 would be ideal but we don’t think this is practical for both time and weight reasons in our urban response service.

Thoracic decompression if hypoxic/shocked & clinical or US suspicion of pneumothorax

I don’t think this one is rocket science. Even if we know a pneumothorax is present on ultrasound we usually leave it alone if they are not compromised. If compromise is present however then we expect it to be decompressed.

If GCS <13, BSL documented

All patients with an altered level of consciousness get their blood glucose documented.

Pelvic binder if shock and:

possible AP compression / Vertical Shear injury or signs of pelvic #

We don’t expect pelvic binders to be placed prophylactically. There is no evidence to support such a practice. We do however think that binders are helpful on AP compression and possibly vertical shear type injuries and the patient is shocked.

So that is it for our multiple blunt trauma bundle. It’s what we came up with on a review of the evidence but we’re always open to clever thoughts from others. If you have comments or suggestions we would love to hear from you.

And next time we return to the Carebundles it might just be time to get to the pointy end of penetrating trauma.

Notes:

As always, we’re very happy to hear other people’s clever takes on things that are worth doing. It helps us re-examine our thinking.

Here’s the PubMed link again for the “a single low blood pressure” matters paper linked above: